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心力衰竭患者中枢性睡眠呼吸暂停的机制。

A mechanism of central sleep apnea in patients with heart failure.

作者信息

Javaheri S

机构信息

Veterans Affairs Medical Center, Department of Medicine, University of Cincinnati College of Medicine, OH 45220, USA.

出版信息

N Engl J Med. 1999 Sep 23;341(13):949-54. doi: 10.1056/NEJM199909233411304.

DOI:10.1056/NEJM199909233411304
PMID:10498490
Abstract

BACKGROUND

Breathing is controlled by a negative-feedback system in which an increase in the partial pressure of arterial carbon dioxide stimulates breathing and a decrease inhibits it. Although enhanced sensitivity to carbon dioxide helps maintain the partial pressure of arterial carbon dioxide within a narrow range during waking hours, in some persons a large hyperventilatory response during sleep may lower the value below the apneic threshold, thereby resulting in central apnea. I tested the hypothesis that enhanced sensitivity to carbon dioxide contributes to the development of central sleep apnea in some patients with heart failure.

METHODS

This prospective study included 20 men who had treated, stable heart failure with left ventricular systolic dysfunction. Ten had central sleep apnea, and 10 did not. The patients underwent polysomnography and studies of their ventilatory response to carbon dioxide.

RESULTS

Patients who met the criteria for central sleep apnea had significantly more episodes of central apnea per hour than those without central sleep apnea (mean [+/-SD], 35+/-24 vs. 0.5+/-1.0 episodes per hour). Those with sleep apnea also had a significantly larger ventilatory response to carbon dioxide than those without central sleep apnea (5.1+/-3.1 vs. 2.1+/-1.0 liters per minute per millimeter of mercury, P=0.007), and there was a significant positive correlation between ventilatory response and the number of episodes of apnea and hypopnea per hour during sleep (r=0.6, P=0.01).

CONCLUSIONS

Enhanced sensitivity to carbon dioxide may predispose some patients with heart failure to the development of central sleep apnea.

摘要

背景

呼吸由一个负反馈系统控制,其中动脉血二氧化碳分压升高会刺激呼吸,而降低则会抑制呼吸。尽管在清醒时对二氧化碳的敏感性增强有助于将动脉血二氧化碳分压维持在较窄范围内,但在某些人身上,睡眠期间过度通气反应过大可能会使该值降至呼吸暂停阈值以下,从而导致中枢性呼吸暂停。我检验了这样一个假设,即对二氧化碳的敏感性增强会促使一些心力衰竭患者发生中枢性睡眠呼吸暂停。

方法

这项前瞻性研究纳入了20名患有经治疗的稳定型心力衰竭且左心室收缩功能障碍的男性。其中10人患有中枢性睡眠呼吸暂停,10人没有。患者接受了多导睡眠图检查以及对二氧化碳通气反应的研究。

结果

符合中枢性睡眠呼吸暂停标准的患者每小时中枢性呼吸暂停发作次数显著多于无中枢性睡眠呼吸暂停的患者(均值[±标准差],每小时35±24次发作 vs. 0.5±1.0次发作)。有睡眠呼吸暂停的患者对二氧化碳的通气反应也显著大于无中枢性睡眠呼吸暂停的患者(每分钟每毫米汞柱5.1±3.1升 vs. 2.1±1.0升,P = 0.007),并且通气反应与睡眠期间每小时呼吸暂停和低通气发作次数之间存在显著正相关(r = 0.6,P = 0.01)。

结论

对二氧化碳的敏感性增强可能使一些心力衰竭患者易发生中枢性睡眠呼吸暂停。

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